Patients with cancer are eligible for hospice care when their life expectancy is 180 days or shorter. This study investigated the prognostic factors of patients with cancer and sepsis who were admitted to an intensive care unit (ICU) to assist with clinical decisions of hospice care. A series of 279 patients admitted to the medical ICU with cancer and sepsis were included. Another series of 109 patients with cancer and sepsis admitted to the other medical ICU in the different branch of our hospital was included to verify the results. Among 279 patients, the 30-, 90-, and 180-day mortality rates were 47.3%, 72.0%, and 81.0%, respectively. APACHE II score and the cancer control status (controlled or remission (CR), active newly diagnosed (AND) and active recurrent or progressive (ARP)) were significant predictors of 30- and 90-day mortality(30-day: AND(odds ratio: 5.66; 95% confidence interval: 2.12-15.15), ARP(6.24; 2.92-13.33), APACHE II( 1.07; 1.03-1.11); 90-day: AND(4.78; 1.91-11.99), ARP( 24.03; 11.11-51.99), APACHE II( 1.07; 1.02-1.19)) and were associated with a poor 180-day outcome. The 180-day mortality were significantly different among the patients with different cancer control status in the series of 279 patients (CR: 29.8%; AND: 69.4%; and ARP: 98.9 %) and that of 109 patients (46.4%; 96.8%; and 94.0%). APACHE II score and the cancer control status may be the prognostic factors for critically ill patients with cancer and sepsis, and they may be helpful for evaluating hospice care.

Background: The BODE index is a multidimensional grading system for predicting the prognoses of patients with chronic obstructive pulmonary disease (COPD). This study investigated whether an amino acids-based metabolic profile developed for heart failure patients (including histidine, ornithine, phenylalanine, and leucine) could identify COPD patients and further discriminates COPD patients in advanced BODE stages. Methods: Ultra-performance liquid chromatography was performed on 119 participants, including 75 COPD patients at different BODE stages and 44 normal controls. Albumin, pre-albumin, transferrin, high sensitivity C-reactive protein, and hand grip strength were also measured. Receiver operating characteristic curves and area under curves were used for estimation. Results: The BODE points in our patients were 3.29 [95% confidence interval (CI) = 2.74–3.85]. Compared to normal controls, COPD patients had lower leucine but higher ornithine levels. A COPD score, developed based on leucine and ornithine, significantly discriminated COPD from normal controls [odds ratio (OR) = 2.71, 95% CI = 1.83–4.04, p <0.001]. A COPD score of ≥ 3.00 had an OR of 15.58 (95% CI = 5.96–40.73, p <0.001). In COPD patients from BODE 1 to BODE 4, the levels of histidine, ornithine and phenylalanine increased significantly. In multivariable analysis, histidine and phenylalanine were independently able to distinguish BODE stages 3 and 4 from BODE 1 and were adopted to develop a metabolic score. Metabolic scores identified patients at BODE 3 and 4 (OR = 2.74, 95% CI =1.41–5.29, p = 0.003) better than hand grip strength, high sensitive C-reactive protein, albumin, pre-albumin, and transferrin value. A metabolic score of ≥9.53 significantly discriminated BODE 3 and 4 from BODE 1 and 2 (OR = 8.56, 95% CI = 2.77–26.39, p <0.001). Conclusion: Amino acid-based COPD score and metabolic score discriminate COPD patients from normal controls, and identify patients in advanced stages of COPD.

Mechanical ventilation (MV) is required to maintain life for patients with sepsis-related acute lung injury but can cause diaphragmatic myotrauma with muscle damage and weakness, known as ventilator-induced diaphragm dysfunction (VIDD). Hypoxia-inducible factor 1α (HIF-1α) plays a crucial role in inducing inflammation and apoptosis. Low-molecular-weight heparin (LMWH) was proven to have anti-inflammatory properties. However, HIF-1α and LMWH affect sepsis-related diaphragm injury has not been investigated. We hypothesized that LMWH would reduce endotoxin-augmented VIDD through HIF-1α. C57BL/6 mice, either wild-type or HIF-1α–deficient, were exposed to MV with or without endotoxemia for 8 h. Enoxaparin (4 mg/kg) was administered subcutaneously 30 min before MV. MV with endotoxemia aggravated VIDD, as demonstrated by increased interleukin-6 and macrophage inflammatory protein-2 levels, oxidative loads, and the expression of HIF-1α, calpain, caspase-3, atrogin-1, muscle ring finger-1, and microtubule-associated protein light chain 3-II. Disorganized myofibrils, disrupted mitochondria, increased numbers of autophagic and apoptotic mediators, substantial apoptosis of diaphragm muscle fibers, and decreased diaphragm function were also observed (p < 0.05). Endotoxin-exacerbated VIDD and myonuclear apoptosis were attenuated by pharmacologic inhibition by LMWH and in HIF-1α–deficient mice (p < 0.05). Our data indicate that enoxaparin reduces endotoxin-augmented MV-induced diaphragmatic injury, partially through HIF-1α pathway inhibition.

Objective: Periodic leg movement in sleep (PLMS) is common among patients with obstructive sleep apnea (OSA). The PLMS frequency changes after continuous positive airway pressure (CPAP) titration. This study investigated the effects of two PLMS diagnostic criteria on PLMS prevalence and the restless leg syndrome (RLS) detection rate in patients with OSA before and after CPAP titration. Methods: This retrospective study included patients with OSA who received polysomnography (PSG) and successful CPAP titration from December 2012 to December 2014. Their clinical variables and sleep parameters were evaluated using the PLMS diagnostic criteria: PLMS index (PLMI) ≥5 and ≥15. PLMS prevalence and the RLS detection rate were analyzed according to the PLMI before and after CPAP. Results: In patients with OSA with a PLMI of ≥5 and ≥15 after PSG with CPAP titration, the PLMS prevalence was 20.1% (76/378) and 4.5% (17/378), respectively, which revealed CPAP titration increased PLMI. Moreover, in terms of PLMI ≥5 and ≥15, PSG with CPAP titration led to significantly higher PLMS prevalence than PSG alone (20.1% vs 7.1% and 4.5% vs 0.8%, respectively; both P<0.001). PLMI ≥5 also demonstrated a higher RLS detection rate than PLMI ≥15 did (69.2% vs 15.4%; P=0.016). Conclusion: In patients with OSA, CPAP titration increases PLMS prevalence and the PLMI regardless of whether PLMI is ≥5 or ≥15. The use of the current diagnostic criteria, PLMI ≥15, for PLMS may lead to underestimation of PLMS prevalence and the RLS detection rate in patients with OSA.

Objectives: To assess the effect of continuous positive airway pressure (CPAP) on nocturia in ischemic stroke patients with obstructive sleep apnea (OSA). Methods: This was a prospective and non-randomized controlled study in which ischemic stroke patients with OSA being treated in a rehabilitation ward were enrolled. The participants who tolerated CPAP were classified as the CPAP group, while those who refused or could not tolerate CPAP were classified as the control group. The percentage change of nocturia before and after 2 weeks of CPAP therapy between the two groups were compared. Results: A total of 44 participants were enrolled in and 35 participants (mean age=59.8±11.7 years old; mean apnea hypopnea index=42.9±16.7/h) completed the study (control group: 14, CPAP group: 21). Overall, 69% of the participants had nocturnal polyuria and 69% of them had more than one nocturia episode per night. The baseline and initial nocturia characteristics did not differ significantly between the two groups. As compared to the control group, CPAP therapy significantly decreased the nocturnal polyuria index (mean percentage change: 9% vs -21% (P=0.005)) and nocturnal urine output (mean percentage change: 6% vs -26% (P=0.04)), but not the nocturia episodes or 24-hours total urine output. Conclusion: Nocturia due to nocturnal polyuria is very common in post-stroke patients with OSA. Treating OSA by CPAP significantly reduces nocturnal polyuria, but not nocturia frequency, in ischemic stroke patients.

Mechanical ventilation (MV) is essential for patients with sepsis-related respiratory failure but can cause ventilator-induced diaphragm dysfunction (VIDD), which involves diaphragmatic myofiber atrophy and contractile inactivity. Mitochondrial DNA, oxidative stress, mitochondrial dynamics, and biogenesis are associated with VIDD. Hypoxia-inducible factor 1α (HIF-1α) is crucial in the modulation of diaphragm immune responses. The mechanism through which HIF-1α and mitochondria affect sepsis-related diaphragm injury is unknown. We hypothesized that MV with or without endotoxin administration would aggravate diaphragmatic and mitochondrial injuries through HIF-1α. C57BL/6 mice, either wild-type or HIF-1α-deficient, were exposed to MV with or without endotoxemia for 8 h. MV with endotoxemia augmented VIDD and mitochondrial damage, which presented as increased oxidative loads, dynamin-related protein 1 level, mitochondrial DNA level, and the expressions of HIF-1α and light chain 3-II. Furthermore, disarrayed myofibrils; disorganized mitochondria; increased autophagosome numbers; and substantially decreased diaphragm contractility, electron transport chain activities, mitofusin 2, mitochondrial transcription factor A, peroxisome proliferator activated receptor-γ coactivator-1α, and prolyl hydroxylase domain 2 were observed (p < 0.05). Endotoxin-stimulated VIDD and mitochondrial injuries were alleviated in HIF-1α-deficient mice (p < 0.05). Our data revealed that endotoxin aggravated MV-induced diaphragmatic dysfunction and mitochondrial damages, partially through the HIF-1α signaling pathway.